Effects of physiological and synthetic IAP antagonism on c-IAP dependent signaling

ABSTRACT: Cellular inhibitor of apoptosis proteins 1 and 2 (c-IAP1/2) play central roles in signal transduction mediated by numerous receptors that participate in inflammatory and immune responses. In certain pathways, such as activation of NF-kB, their degradation is a major regulatory event and is physiologically induced by activation of receptors. Additionally, a number of synthetic compounds have been developed that also target the c-IAPs and induce their degradation. However, the extent of a synthetic IAP antagonist’s ability to mirror the transcriptional program by a physiological signal remains unclear. Here we take a systems approach to compare the transcriptional programs triggered by activation of CD30, a well-characterized receptor previously shown to induce the degradation of the c-IAPs,

ORGANISM(S): Homo sapiens

SUBMITTER: Mats Ljungman 

PROVIDER: E-GEOD-64927 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress